Effects of a Vegetarian, Supplemented Diet on Renal Function, Proteinuria, and Glucose Metabolism in Patients with �Overt� Diabetic Nephropathy and Renal Insufficiency

Author(s):  
G. Barsotti ◽  
R. Navalesi ◽  
O. Giampietro ◽  
F. Ciardella ◽  
E. Morelli ◽  
...  

1997 ◽  
Vol 43 (6) ◽  
pp. 17-20
Author(s):  
Yu. I. Grinshtein ◽  
S. V. Ivliev ◽  
N. B. Osetrova ◽  
S. S. Ilyenkov

The conjunctival bloodflow was examined in patients with diabetic nephropathy with different status of renal function and changes in the microcirculatory bed assessed after endovascular laser therapy. Twenty-five donors and twenty-one patients with medium-severe and grave type I diabetes complicated by diabetic nephropathy were followed up. Microcirculatory disorders in the eyeball conjunctiva progressed as renal function deteriorated, which was evident from a reliable increase of the total conjunctival index in parallel with the progress of chronic- renal insufficiency. A course of endovascular laser therapy reliably improved the microcirculation: the arterio-venular coefficient increased and the total conjunctival index decreased in patients with latent and conservatively curable stages of chronic renal insufficiency due to normalization of vascular tone, boosting of the bloodflow, and decrease of red cell sludging.



1996 ◽  
Vol 42 (2) ◽  
Author(s):  
M. V. Shestakova ◽  
M. Sh. Shamkhalova ◽  
T. T. Ukhanova ◽  
M. G. Ryndina ◽  
I. I. Dedov

Study of the effects of glurenorm, an oral sugar- reducing drug, on renal function and vascular endothelium in patients with noninsulin-dependent diabetes mellitus at different stages of diabetic involvement of the kidneys, including those with chronic renal insufficiency, revealed that glurenorm in therapeutic doses had no nephrotoxic effect; moreover, it maintained the filtration function of the kidneys even in patients with the initial stage of chronic renal insufficiency (with blood serum creatinine of up to 200 mmol/liter. Therapy with glurenorm for 3 and 6 months caused a reliable reduction of the production of thromboxane A, a vasoconstrictor, this probably improving the intrarenal hemodynamics, and exerting an antiproteinuric effect in patients with manifest diabetic nephropathy. At the same time, glurenorm therapy did not appreciably influence the production of factors released by vascular endothelium (prostacyclin and endothelin-1). Hence, a detailed study of renal function and vascular endothelium in patients with type II diabetes demonstrated that administration of glurenorm to patients with manifest renal involvement was not only safe, but even favorably affected the intrarenal hemodynamics and had an antiproteinuric effect.



2010 ◽  
Vol 13 (4) ◽  
pp. 87-92
Author(s):  
Irina Arkad'evna Bondar' ◽  
Vadim Valer'evich Klimontov

Diabetes mellitus (DM) is a leading cause of renal insufficiency in developed countries. Most cases of chronic renal disease in DM patients are dueto diabetic nephropathy. The impairment of renal function at later stages of diabetic nephropathy is accompanied by complicated changes in the regulationof carbohydrate metabolism most of which require hypoglycemic therapy to be corrected



1989 ◽  
Vol 61 (03) ◽  
pp. 522-525 ◽  
Author(s):  
M P Gordge ◽  
R W Faint ◽  
P B Rylance ◽  
H Ireland ◽  
D A Lane ◽  
...  

SummaryD dimer and other large fragments produced during the breakdown of crosslinked fibrin may be measured by enzyme immunoassay using monoclonal antibodies. In 91 patients with renal disease and varying degrees of renal dysfunction, plasma D dimer showed no correlation with renal function, whereas FgE antigen, a fibrinogen derivative which is known to be cleared in part by the kidney, showed a significant negative correlation with creatinine clearance. Plasma concentrations of D dimer were, however, increased in patients with chronic renal failure (244 ± 3l ng/ml) (mean ± SEM) and diabetic nephropathy (308 ± 74 ng/ml), when compared with healthy controls (96 ± 13 ng/ml), and grossly elevated in patients with acute renal failure (2,451 ± 1,007 ng/ml). The results indicate an increase in fibrin formation and lysis, and not simply reduced elimination of D dimer by the kidneys, and are further evidence of activated coagulation in renal disease. D dimer appears to be a useful marker of fibrin breakdown in renal failure.



1986 ◽  
Vol 56 (02) ◽  
pp. 229-231 ◽  
Author(s):  
A H Hopper ◽  
H Tindall ◽  
J A Davies

SummaryTBeta-thromboglobulin (βTG) is a platelet-specific protein and since its concentration in plasma rises when platelets are activated, it has been used as an indicator of platelet involvement in vascular disease. Since platelets might be involved in the pathogenesis of diabetic microvascular disease we measured urinary βTG in 20 insulin-dependent diabetics with nephropathy and compared the results with those from 20 normal subjects. Measurement of βTG in urine was undertaken to avoid errors induced by blood sampling and to gain information over a prolonged period using a single assay. Measurements were made of βTG, β2-microglobulin and total protein in urine collected for 24 h and creatinine and β2 microglobulin in plasma. Survival of indium-111-labelled platelets was measured in nine patients. Urinary PTG was significantly (p <0.02) increased in the 20 patients compared with 20 normal volunteers (median value 1.3 vs 0.8 μg/24 h). There was a strong correlation between urinary βTG excretion and plasma creatinine concentration (r = 0.8, p <0.0001) and plasma β2-microglobulin concentration (r = 0.9, p <0.0001). Urinary βTG concentration did not correlate with platelet survival. The results indicate that although urinary βTG is significantly increased in patients with diabetic nephropathy its concentration in urine correlates with indicators of glomerular filtration rather than with a test of platelet activation.



2007 ◽  
Vol 115 (S 1) ◽  
Author(s):  
W Reinhardt ◽  
U Ewerhart ◽  
K Mann ◽  
O Witzke


2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Narongrit Siriwattanasit ◽  
Bancha Satirapoj ◽  
Ouppatham Supasyndh

Abstract Background Activation of the transforming growth factor beta (TGF-β) pathway is a significant contributor to the pathogenesis of diabetic nephropathy. Carnosine is a dipeptide that can inhibit TGF-β synthesis. We tested the hypothesis that carnosine supplement added to standard therapy will result in reduced urinary TGF-β levels among patients with diabetic nephropathy. Methods We randomly assigned 40 patients with diabetic nephropathy and albuminuria 30–299 mg/day to treatment with carnosine (2 g/day) or placebo for 12 weeks. Urinary TGF-β level was determined using ELISA, urine albumin was ascertained by immunonephelometric assay, and renal function and metabolic profiles were determined at baseline and during 12 weeks of active treatment. Primary outcome was decrease in urinary levels of TGF-β. Results The 2 groups were comparable for baseline characteristics, blood pressure, urine albumin, urine TGF-β and renal function measurements. Urinary TGF-β significantly decreased with carnosine supplement (− 17.8% of the baseline values), whereas it tended to increase with placebo (+ 16.9% of the baseline values) (between-group difference P < 0.05). However, blood urea nitrogen, serum creatinine, glomerular filtration rate and other biochemical parameters remained unchanged during the study period including urinary albuminuria. Both groups were well tolerated with no serious side-effects. Conclusions These data indicated an additional renoprotective effect of oral supplementation with carnosine to decrease urinary TGF-β level that serves as a marker of renal injury in diabetic nephropathy. Trial registration Thai Clinical Trials, TCTR20200724002. Retrospectively Registered 24 July 2020.



2020 ◽  
Vol 7 (Supplement_1) ◽  
pp. S605-S605
Author(s):  
Pierre Bulpa ◽  
Galia Rahav ◽  
Ilana Oren ◽  
Mickaël Aoun ◽  
George R Thompson ◽  
...  

Abstract Background Fosmanogepix (FMGX) is a first-in-class antifungal agent, with a unique MOA targeting the fungal enzyme Gwt1, and broad-spectrum activity against yeasts and molds, including fungi resistant to other antifungal agents. Patients with candidemia often have underlying renal insufficiency or are receiving medications that affect renal function. This analysis evaluated outcomes in patients with varying degrees of renal insufficiency. Methods This global, multicenter, open-label, non-comparative study evaluated the safety and efficacy of FMGX for first-line treatment of candidemia. Patients with a recent diagnosis of candidemia defined as positive blood culture for Candida spp within 96 hrs prior to study entry with ≤ 2 days of prior antifungal treatment were eligible, including those with renal insufficiency. Patients with neutropenia, C. krusei infection, deep-seated Candida infections or receiving hemodialysis were excluded. Subjects were treated with FMGX for up to 14 days: 1000 mg IV BID for 1 day, then 600 mg IV QD for at least 2 days, followed by either 600 mg IV QD or 700 mg PO QD. Patients requiring antifungal treatment beyond 14 days received fluconazole. The primary efficacy endpoint was outcome at end of study treatment (EOST) as determined by an independent data review committee. Successful outcome was defined as survival with clearance of Candida from blood cultures with no additional antifungal treatment. Results 14/21 (66%) subjects had some degree of renal insufficiency: 7 had mild renal insufficiency (GFR:60-89), 5 had moderate renal insufficiency (GFR:30-59), and 2 had severe renal insufficiency (GFR:15-29). 12/14 (86%) completed study treatment, and treatment was successful at EOST in 12/14 (86%) subjects. Decline in renal function was not observed at EOST. 4 had worsening of renal function during the follow-up period; none required dialysis. Renal impairment did not increase exposure of FMGX. There were no treatment-related adverse events. Conclusion FMGX demonstrated high level treatment success with no evidence of drug-related nephrotoxicity, with no dose adjustments required. These preliminary data support the continued evaluation of FMGX in patients with candidemia and renal dysfunction as an alternative to potentially nephrotoxic antifungal agents. Disclosures Pierre Bulpa, MD, Amplyx Pharmaceuticals (Scientific Research Study Investigator) Galia Rahav, MD, AstraZeneca (Scientific Research Study Investigator) Mickaël Aoun, MD, Amplyx Pharmaceuticals (Scientific Research Study Investigator) Peter Pappas, MD, SCYNEXIS, Inc. (Consultant, Advisor or Review Panel member, Research Grant or Support) Bart Jan Kullberg, MD, FRCP, FIDSA, Amplyx (Advisor or Review Panel member) Sara Barbat, BSN, RN, Amplyx Pharmaceuticals (Employee) Pamela Wedel, BSc, Amplyx Pharmaceuticals (Employee) Haran T. Schlamm, MD, Amplyx (Consultant) Michael Hodges, BSc. MD, Amplyx Pharmaceuticals Inc. (Employee)







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